| pubmed-article:19079240 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19079240 | lifeskim:mentions | umls-concept:C0041625 | lld:lifeskim |
| pubmed-article:19079240 | lifeskim:mentions | umls-concept:C1704410 | lld:lifeskim |
| pubmed-article:19079240 | lifeskim:mentions | umls-concept:C0205191 | lld:lifeskim |
| pubmed-article:19079240 | pubmed:issue | 7229 | lld:pubmed |
| pubmed-article:19079240 | pubmed:dateCreated | 2009-1-29 | lld:pubmed |
| pubmed-article:19079240 | pubmed:abstractText | In nature, organisms are exposed to chronic low-dose ultraviolet light (CLUV) as opposed to the acute high doses common to laboratory experiments. Analysis of the cellular response to acute high-dose exposure has delineated the importance of direct DNA repair by the nucleotide excision repair pathway and for checkpoint-induced cell cycle arrest in promoting cell survival. Here we examine the response of yeast cells to CLUV and identify a key role for the RAD6-RAD18-RAD5 error-free postreplication repair (RAD6 error-free PRR) pathway in promoting cell growth and survival. We show that loss of the RAD6 error-free PRR pathway results in DNA-damage-checkpoint-induced G2 arrest in CLUV-exposed cells, whereas wild-type and nucleotide-excision-repair-deficient cells are largely unaffected. Cell cycle arrest in the absence of the RAD6 error-free PRR pathway was not caused by a repair defect or by the accumulation of ultraviolet-induced photoproducts. Notably, we observed increased replication protein A (RPA)- and Rad52-yellow fluorescent protein foci in the CLUV-exposed rad18Delta cells and demonstrated that Rad52-mediated homologous recombination is required for the viability of the rad18Delta cells after release from CLUV-induced G2 arrest. These and other data presented suggest that, in response to environmental levels of ultraviolet exposure, the RAD6 error-free PRR pathway promotes replication of damaged templates without the generation of extensive single-stranded DNA regions. Thus, the error-free PRR pathway is specifically important during chronic low-dose ultraviolet exposure to prevent counter-productive DNA checkpoint activation and allow cells to proliferate normally. | lld:pubmed |
| pubmed-article:19079240 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19079240 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:19079240 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:19079240 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19079240 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:19079240 | pubmed:issn | 1476-4687 | lld:pubmed |
| pubmed-article:19079240 | pubmed:author | pubmed-author:CarrAntony... | lld:pubmed |
| pubmed-article:19079240 | pubmed:author | pubmed-author:IwasakiHirosh... | lld:pubmed |
| pubmed-article:19079240 | pubmed:author | pubmed-author:HishidaTakash... | lld:pubmed |
| pubmed-article:19079240 | pubmed:author | pubmed-author:KubotaYoshino... | lld:pubmed |
| pubmed-article:19079240 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19079240 | pubmed:day | 29 | lld:pubmed |
| pubmed-article:19079240 | pubmed:volume | 457 | lld:pubmed |
| pubmed-article:19079240 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19079240 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19079240 | pubmed:pagination | 612-5 | lld:pubmed |
| pubmed-article:19079240 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:19079240 | pubmed:year | 2009 | lld:pubmed |
| pubmed-article:19079240 | pubmed:articleTitle | RAD6-RAD18-RAD5-pathway-dependent tolerance to chronic low-dose ultraviolet light. | lld:pubmed |
| pubmed-article:19079240 | pubmed:affiliation | Research Institute for Microbial Diseases, Osaka University, 3-1 Yamadaoka, Suita, Osaka 565-0871, Japan. hishida@biken.osaka-u.ac.jp | lld:pubmed |
| pubmed-article:19079240 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:19079240 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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